Mitochondrial function assessed by 31P MRS and BOLD MRI in non-obese type 2 diabetic rats.
Mitochondrial function assessed by 31P MRS and BOLD MRI in non-obese type 2 diabetic rats.
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DOI：
10.14814/phy2.12890
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发表时间：
2016-08
影响因子：
2.5
通讯作者：
Yu X
中科院分区：
文献类型：
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作者：
Liu Y;Mei X;Li J;Lai N;Yu X
本研究旨在通过评价后藤-Kakizaki（GK）大鼠（一种非肥胖型2型糖尿病（T2 D）大鼠模型）骨骼肌对缺血-再灌注的反应，表征骨骼肌生物能量学的年龄相关变化。对年轻（12周）和成年（20周）GK和Wistar（对照）大鼠的后肢进行31 P磁共振波谱（MRS）和血氧水平依赖性（BOLD）MRI。在缺血和再灌注方案期间连续采集31 P-MRS和BOLD-MRI数据，以量化磷酸盐代谢物和肌肉氧合的变化。磷酸肌酸恢复的时间常数（线粒体氧化能力的指标）在GK大鼠（年轻组60.8 ± 13.9秒，成年组83.7 ± 13.0秒）与其年龄匹配的对照组（年轻组62.4 ± 11.6秒，成年组77.5 ± 7.1秒）之间无统计学差异。在缺血期间，GK大鼠的基线标准化BOLD-MRI信号显著低于其年龄匹配的对照组。这些结果表明，胰岛素抵抗导致GK大鼠组织代谢的改变，而不损害线粒体氧化能力。
The study aims to characterize age‐associated changes in skeletal muscle bioenergetics by evaluating the response to ischemia‐reperfusion in the skeletal muscle of the Goto‐Kakizaki (GK) rats, a rat model of non‐obese type 2 diabetes (T2D). 31P magnetic resonance spectroscopy (MRS) and blood oxygen level‐dependent (BOLD) MRI was performed on the hindlimb of young (12 weeks) and adult (20 weeks) GK and Wistar (control) rats. 31P‐MRS and BOLD‐MRI data were acquired continuously during an ischemia and reperfusion protocol to quantify changes in phosphate metabolites and muscle oxygenation. The time constant of phosphocreatine recovery, an index of mitochondrial oxidative capacity, was not statistically different between GK rats (60.8 ± 13.9 sec in young group, 83.7 ± 13.0 sec in adult group) and their age‐matched controls (62.4 ± 11.6 sec in young group, 77.5 ± 7.1 sec in adult group). During ischemia, baseline‐normalized BOLD‐MRI signal was significantly lower in GK rats than in their age‐matched controls. These results suggest that insulin resistance leads to alterations in tissue metabolism without impaired mitochondrial oxidative capacity in GK rats.